Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatolactin (SL), a recently identified teleost pituitary hormone which is a member of the growth hormone/prolactin family, was isolated from pituitary tissue of Atlantic halibut (Hippoglossus hippoglossus). Pituitary proteins were extracted in ammonium bicarbonate (pH 7.8), fractionated using gel filtration chromatography, and purified using reversed-phase high-performance liquid chromatography. Halibut SL was identified on the basis of molecular size (determined by gel electrophoresis and mass spectroscopy), cross-reactivity of the putative hormone with antisera to cod SL, and N-terminal amino acid sequence. Polyclonal antibodies to purified halibut SL were raised in rabbits, and a radioimmunoassay (RIA) was developed for measurement of plasma concentrations of SL using purified halibut SL as a standard. The RIA was tested in several flatfish species including Pacific halibut (Hippoglossus stenolepis), English sole (Pleuronectes vetulus), and rock sole (Lepidopsetta bilineata). The assay was specific for SL as indicated by absence of cross-reactivity with Atlantic halibut growth hormone, prolactin, and GTH alpha subunit. Dilutions of plasma and pituitary extracts from Pacific halibut, English sole, and rock sole were parallel to the Atlantic halibut SL standard curve, indicating that the assay is valid for a range of flatfish species. Using halibut SL antiserum, SL was localized in the pars intermedia of English sole pituitary, where it has been identified in previously examined teleost species. The RIA was used to measure plasma levels of SL in Atlantic halibut and English sole during reproductive development, and in English sole subjected to various types of environmental stressors, including handling and crowding. In both sole and halibut, plasma SL concentrations remained relatively constant throughout gonadal development, but dropped during or following ovulation. Plasma SL levels in English sole tended to increase in response to acute stress, in parallel with plasma cortisol levels.
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PMID:Isolation, characterization, and radioimmunoassay of Atlantic halibut somatolactin and plasma levels during stress and reproduction in flatfish. 903 52

Cortisol response to stress appears to differ between lactating and non-lactating animals. Lactating (14 d post partum) and non-lactating sheep were fitted with probes so that drugs and hormones could be infused directly into the posterior pituitary and paraventricular nucleus of the hypothalamus. The animals were also fitted with instruments to allow monitoring of heart rate, body temperature and blood cortisol levels. Their reactions to a source of acute stress (a barking dog) were then followed, with or without drug and hormone manipulation. Results in both lactating and non-lactating animals indicated shortcomings in the use of cortisol as a stress indicator. Infusing prolactin and oxytocin into either the posterior pituitary or the paraventricular nucleus of the hypothalamus suppressed cortisol responsiveness to stress in both lactating and non-lactating animals (the latter to a greater extent). In the absence of drugs, lactating animals had a slightly higher basal level of cortisol and a lower cortisol response to stress than their non-lactating counterparts. Despite suppression of cortisol responses, with or without drugs, other indicators of stress still changed with the presence of a barking dog, suggesting the complexity of control involved in stress responses.
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PMID:Oxytocin and prolactin suppress cortisol responses to acute stress in both lactating and non-lactating sheep. 927 53

Vasoactive intestinal peptide (VIP) is a potent releaser of prolactin (PRL) in domestic fowl, turkey, and ring doves. However, few comparative studies have investigated this in wild species. We tested the effects of intravenously administered chicken VIP on plasma PRL concentrations in four passerine species: the white-crowned sparrow (Zonotrichia leucophrys gambelii), the dark-eyed junco (Junco hyemalis), the Florida scrub-jay (Aphelocoma coerulescens), and the western scrub-jay (A. californica). In the white-crowned sparrow, junco, and Florida scrub-jay, which were tested during the breeding season, VIP induced a rapid increase in plasma PRL. Serial plasma samples taken after VIP injection in the white-crowned sparrow show a 10-fold increase in PRL within 2 min of treatment, followed by a gradual decline. Effects of VIP, as compared to saline, remained significant for at least 20 min after treatment. Western scrub-jays did not respond to intravenous VIP with a significant rise in PRL secretion, possibly because they were tested after termination of the breeding season. This study indicates that VIP control of PRL release may be widespread among avian species, and that seasonal changes in plasma PRL may be mediated in part at the level of the pituitary. In addition, analysis of the control data revealed no increase in plasma PRL as a result of injection or restraint, suggesting that unlike in mammals, PRL is not released during acute stress in passerines.
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PMID:Effects of vasoactive intestinal peptide on plasma prolactin in passerines. 1006 94

An unexplained hallmark of prolonged critical illness is the fact that food does not prevent or reverse protein wasting, while fat is paradoxically accrued. This 'wasting syndrome' often persists after the underlying disease has been resolved and thus perpetuates intensive care dependency. Although the crucial role of an intact hypothalamus-pituitary axis for homeostasis during stress is well recognized, the differences between the neuroendocrine changes observed in acute and prolonged critical illness were only recently described. Novel insights in this area are reviewed here. The initial endocrine stress response consists primarily of a peripheral inactivation of anabolic pathways while pituitary activity is essentially amplified or maintained. These responses presumably provide the metabolic substrates and host defense required for survival and to delay anabolism, and thus should be considered as adaptive and beneficial. Persistence of this acute stress response throughout the course of critical illness was hitherto assumed. This assumption has now been invalidated, since a uniformly reduced pulsatile secretion of ACTH, TSH, LH, prolactin (PRL) and GH has been observed in protracted critical illness, causing diminished stimulation of several target organs. Impaired pulsatile secretion of anterior pituitary hormones in the chronic phase of critical illness seems to have a hypothalamic rather than a pituitary origin, as administration of relevant releasing factors evoked immediate and pronounced pituitary hormone release. A reduced availability of TRH, one of the endogenous ligands of the GH-releasing peptide (GHRP) receptor (such as the recently discovered ghrelin) and, in very long-stay critically ill men, also of GHRH, appear to be involved. This hypothesis was further explored by investigating the effects of continuous i.v. infusion of GHRH, GHRP, TRH and their combinations for several days. Pulsatile secretion of GH, TSH and PRL was re-amplified by relevant combinations of releasing factors which also substantially increased circulating levels of IGF-I, GH-dependent binding proteins, thyroxine and tri-iodothyronine (T3) while avoiding a rise in reverse T3. Active feedback-inhibition loops prevented overstimulation of target organs and metabolic improvement was noted with the combined infusion of GHRP and TRH. Whether this novel endocrine strategy will also enhance clinical recovery from critical illness remains to be explored.
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PMID:Novel insights into the neuroendocrinology of critical illness. 1087 25

The cellular organization of the paraventricular nucleus (PVN) is complex and eight distinct regions have been identified by Nissl staining. Three consist of magnocellular neurons and five of parvocellular neurons. Ibotenic acid, a glutamate analogue, is a toxin with neuroexcitatory properties which acts on N-methyl-D-aspartate and metabotropic receptors. Depending on the dose used, ibotenic acid causes extensive damage of parvocellular neurons of the paraventricular nucleus but preserves magnocellular neurons and passage fibers, in contrast to electrolytic lesions, which causes diffuse and nonspecific destruction. We studied the prolactin (PRL) and corticosterone secretion in response to acute stress induced by exposure to the ether, 3 weeks after selective neurotoxic lesion of parvocellular neurons of the paraventricular nucleus by microinjection of ibotenic acid. There was no significant difference in the basal levels of PRL and corticosterone between control and lesioned animals. The plasma PRL increased in the sham and lesioned groups after stress of similar manner. However, the increase in plasma corticosterone in response to stress was significantly higher in lesioned animals. In conclusion, the selective lesion of parvocellular neurons of the PVN did not change basal or stress induced PRL secretion but it caused hypersensitivity of the hypothalamus-pituitary-adrenal axis 3 weeks later, probably by corticotropin releasing hormone (CRH) from hypothalamic areas others than parvocellular neurons of the PVN; hypersensitivity of corticotropes to the secretagogues others than CRH; or hyperresponsiveness of AVP receptors in the adenohypophysis. Furthermore, we cannot rule out a putative inhibitory factor of the hypothalamus-pituitary axis produced by parvocellular neurons of the PVN. This factor modulator of corticotropin secretion could be absent after recuperation of the response of the hypothalamus-pituitary axis to the stress.
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PMID:Prolactin and corticosterone secretion in response to acute stress after paraventricular nucleus lesion by ibotenic acid. 1097 87

The initial neuroendocrine response to critical illness illness consists primarily of activated anterior pituitary function, the peripheral anabolic pathways being inactivated. This response presumably provides metabolic substrates, establishes the host's defences and is thus considered to be adaptive and beneficial. It was previously assumed that the acute stress response persisted throughout the course of critical illness, but this assumption has now been disproved. Indeed, a uniformly reduced pulsatile secretion of growth hormone, thyroid-stimulating hormone, prolactin and luteinizing hormone has been observed in protracted critical illness, impairing the function of target organs. A reduced availability of thyrotropin-releasing hormone, gonadotropin-releasing hormone, the endogenous ligand of the growth hormone-releasing peptide receptor (possibly ghrelin) and, in very long-stay critically ill men, also growth hormone-releasing hormone seems to be involved. The pulsatile secretion of growth hormone, thyroid-stimulating hormone, prolactin and luteinizing hormone can be re-established by relevant combinations of releasing factors, which also substantially increase the circulating levels of insulin-like growth factor-1, growth hormone dependent binding proteins, thyroxine, tri-iodothyronine and testosterone. Active feedback inhibition loops prevent the target organs being overstimulated. The metabolism is altered in a beneficial way when growth hormone-secretagogues, thyrotropin-releasing hormone and gonadotropin-releasing hormone are administered together, whereas the effect of single-hormone treatment is minor and accompanied by side-effects. This new concept of a selectively reduced stimulation of pituitary function in the chronic phase of critical illness unveils new therapeutic perspectives to reverse the paradoxical wasting syndrome' and intensive care dependency.
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PMID:The neuroendocrine response to stress is a dynamic process. 1180 May 14

Rats with excitotoxic neonatal ventral hippocampal lesions (NVHL) manifest in early adulthood a variety of behavioral and neurochemical abnormalities mimicking those seen in patients with schizophrenia. Some of these aberrations implicate malfunction of the midbrain dopamine systems. We studied NVHL effects on dopamine release in the rat frontal cortex, nucleus accumbens, and striatum during acute stress caused by inescapable continuous footshock (0.45 mA). Serum total corticosterone and prolactin levels were used as peripheral indices of stress. As an indirect index of dopamine release, tissue 3-methoxytyramine levels attained in vivo 10 min after monoamine oxidase inhibition was assayed in rats sacrificed by instantaneous microwave fixation of the brain tissue. Nonshocked NVHL rats showed significantly less nucleus accumbens' 3-methoxytyramine accumulation than their sham counterparts. Frontal cortical 3-methoxytyramine levels rose similarly after 20-min footshock in both groups of rats, but while it normalized after 60-min footshock in the sham rats, it did not decrease in the NVHL rats. Nucleus accumbens' 3-methoxytyramine was significantly elevated after either 20-min or 60-min footshock in both groups, whereas striatal 3-methoxytyramine was significantly elevated in the NVHL rats only. Serum corticosterone showed similar elevations in the sham and NVHL rats, but the patterns differed in that there was no attenuation after 60-min footshock in the latter. The lesion did not affect serum prolactin response. These data indicate that neonatal ventral hippocampal damage enhances and prolongs certain neural and neuroendocrine responses to acute physical stressor(s), and thus may affect adaptation and enhance detrimental effects of stress.
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PMID:Neonatal ventral hippocampal damage modifies serum corticosterone and dopamine release responses to acute footshock in adult Sprague-Dawley rats. 1253

The cyclooxygenase (COX) pathway converts arachidonic acid (ArA) into prostaglandins (PGs), which interact with the stress response in mammals and possibly in fish as well. Acetylsalicylic acid (ASA) is a COX inhibitor and was used to characterize the effects of PGs on the release of several hormones and the stress response of tilapia (Oreochromis mossambicus). Plasma PGE2 was significantly reduced at 100 mg ASA/kg body wt, and both basal PGE2 and cortisol levels correlated negatively with plasma salicylate. Basal plasma 3,5,3'-triiodothyronine (T3) was reduced by ASA treatment, whereas prolactin (PRL)188 increased at 100 mg ASA/kg body wt. ASA depressed the cortisol response to the mild stress of 5 min of net confinement. As expected, glucose and lactate were elevated in the stressed control fish, but the responses were blunted by ASA treatment. Gill Na+-K+-ATPase activity was not affected by ASA. Plasma osmolarity increased after confinement in all treatments, whereas sodium only increased at the high ASA dose. This is the first time ASA has been administered to fish in vivo, and the altered hormone release and the inhibition of the acute stress response indicated the involvement of PGs in these processes.
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PMID:Effects of acetylsalicylic acid treatment on thyroid hormones, prolactins, and the stress response of tilapia (Oreochromis mossambicus). 1284 67

The role of vasopressin, cosecreted with corticotropin-releasing hormone (CRH), in stress is debated, because both normal as well as reduced adrenocorticotropin hormone (ACTH) rise to an acute challenge has been reported in Brattleboro rats genetically lacking vasopressin (di/di). Because di/di pups could be born either from di/+ (heterozygous) or from di/di mothers, and maternal influence is known to modify adult responsiveness, we investigated whether the influence of maternal genotype could explain the variability. Adult rats from mothers with different genotypes were stressed with 60 min restraint and trunk blood was collected for measuring hormone content by radioimmunoassay at the end of stress. All offspring of di/+ mothers had similar ACTH responses to restraint, while the di/di rats born to, and raised by di/di mothers showed reduced ACTH reactivity to restraint. The di/di rats showed elevated water turnover and required a daily cage cleaning every day, which meant frequent handling. To offset the role of handling, all rats had daily cage cleaning in the next series, but the results were the same as in the first series. To investigate whether lactation, the behaviour of the mother or some other factor during the pregnancy is responsible for the differences, pups from di/+ dams were raised by di/di foster mothers and vice versa. We found that the genotype of parental mother is more important than that of the foster mother. The corticosterone and prolactin elevation normally seen after acute stress was unchanged by family history, maternal or personal genotype. Furthermore, in studies with mutant animals, the rearing conditions should be controlled by the experimenter. In experiments with Brattleboro rats, the use of homozygous and heterozygous rats from the same litters of di/+ dams and di/di males is recommended. Our results suggest that vasopressin is not indispensable for ACTH release, and that the di/di genotype of the parental mother can decrease the stress reactivity of the di/di Brattleboro rats.
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PMID:Maternal genotype influences stress reactivity of vasopressin-deficient brattleboro rats. 1463 71

Stress causes hypocalcemia and ulcerogenesis in rats. In rats under stressful conditions, a rapid and transient increase in circulating prolactin (PRL) is observed, and this enhanced PRL induces PRL receptors (PRLR) in the choroid plexus of rat brain. In this study we used restraint stress in water to elucidate the mechanism by which PRLR in the rat brain mediate the protective effect of PRL against stress-induced hypocalcemia and ulcerogenesis. We show that rat PRL acts through the long form of PRLR in the hypothalamus. This is followed by an increase in the long form of PRLR mRNA expression in the choroid plexus of the brain, which provides protection against restraint stress in water-induced hypocalcemia and gastric erosions. We also show that PRL induces the expression of PRLR protein and corticotropin-releasing factor mRNA in the paraventricular nucleus. These results suggest that the PRL levels increase in response to stress, and it moves from the circulation to the cerebrospinal fluid to act on the central nervous system and thereby plays an important role in helping to protect against acute stress-induced hypocalcemia and gastric erosions.
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PMID:Prolactin prevents acute stress-induced hypocalcemia and ulcerogenesis by acting in the brain of rat. 1471 16


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